Alzheimer 's Disease : The Most Widespread Age Related Neurodegenerative Diseases

Proteinaceous Infectious Particles, commonly known as Prions, are extremely rare misfolds of the protein PrPc, which cause fatally neurodegenerative diseases, and are theorized to be infectious only by the protein itself (U.S National Library of Medicine, 1998). This “protein-only theory” is still heavily debated today, as some scientists deny the theory, and there isn’t a significant amount of evidence on each side to qualify the theory or disprove it (Soto, C. 2011). The base “Prion” protein is encoded in the gene PRNP, while being non-infectious. Prions are most commonly found in human prion diseases, but they can also be in other animals in the form of Mad Cow Disease and Chronic Wasting Disease, classified as Bovine Spongiform Encephalopathies

The disease stem cells could fix is called Alzheimer’s Disease (AD). The reason I chose this topic is because I have seen first hand how badly someone who suffers from Alzheimer’s Disease is affected in their daily lives. This disease completely takes over their lives and they turn into a completely different person who can hardly function. AD is very tough on the loved ones of the person suffering from it because that person, most of the time has no idea what is going on or who their loved ones are. The memories for people with AD is completely gone and even the simplest tasks such as remembering to use the bathroom becomes difficult. The way stem cells could be feasible is because stem cell-based therapies could potentially treat

Alzheimer 's disease (AD) is a progressive degenerative disease of the brain from which there is no recovery. There are three brain abnormalities that are the hallmarks of the Alzheimer’s disease is initially caused by plaques buildup in the brain’s neurons as illustrated in figure 1. The support structure that allows the flow of the nutrients through the neurons gets damaged and ultimately there is loss of connection among the neurons and they die off (National Institute of Health, 2015). This causes the brain tissue to shrinks, which is called atrophies. All this ultimately lead the victim of this disease to face difficulties in governing emotions, recognize errors and patterns, coordinate movement, and remember. Ultimately, a person with AD loses all memory and mental functioning.

Alzheimer’s Disease has been one of the top leading causes of death in our country. It is understood that this disease is identified as an excess of the protein amyloid-ß within an increase of plaque (Seneff, Wainwright, and Mascitelli, 2010). Additionally, as the brain ages, it gets used to the inflammation and oxidative stress, so it is important to take the right amount of antioxidant micronutrients like vitamin C and vitamin E as well as anti-inflammatory macronutrients such as omega-3 polyunsaturated fatty acids to protect the brain from ageing (Whalley et. al, 2004). This is a devastating disease that affects most people over the age of fifty. Recently, there have been many studies done to figure out what causes this disease, if there is anything that can cure it, and how to prevent the disease. Seneff, Wainwright, and Mascitelli, believe Alzheimer’s develops with consuming too many carbohydrates, especially fructose and having a deficiency in cholesterol and dietary fats as well (2010). Whalley, Starr, and Deary have seen that poor diet, poverty, and failing health are links to developing Alzheimer’s Disease (2004). Furthermore, seeing increase in plasma homocysteine concentration increases risk of Dementia, which can result from an inadequate intake of vitamin B12/folate (Walley et. al, 2004). Additionally, Gray supports Walley’s findings and even believes having an adequate intake of vitamin B12/folate will have a positive effect on the overall health

Alzheimer’s disease is a prominent brain disease that effects a massive amount of individuals in the United States. Alzheimer’s disease (AD) is the sixth leading cause of death in the United States, accounting for 60-80% of dementia cases, with no chance of being cured, prevented or decelerating over time (Alzheimer’s Association, 2014). AD is the most well-known form of dementia, causing complications in brain function in the areas of memory, thinking, and behavior (Alzheimer’s Association, 2014). In an effort to gain a deeper understanding of Alzheimer’s disease, researchers create new knowledge about the disease, which is then distributed to the public. The goal in this information disbursement is to find new and inventive ways to treat AD, prevent AD from progressing at such a rapid pace, and aid in the quality of life in those diagnosed with AD as well as caregivers and medical professionals providing treatment to individuals’ with AD.

A brain deteriorates, slowly being engulfed by a mysterious disease. The neurons being cut off and destroyed by two abnormal structures. First memory is affected gradually getting worse. Then one is unable to think properly, reason, and lacks of self control. Gaps are formed in the brain 's ventricles, due to the amount of dead tissue. In the end, it will lead to death. All of this may sound like something from a science fiction movie but infact its very real. These are all known possible symptoms of a common disease that affects about millions of Americans. It is known as Alzheimer 's disease (AD), and I plan on explaining it a bit more in this paper. First I will explain the disease and list some facts about it,then I will talk about some commonly asked questions about it.

First discovered, while Alois was preforming an autopsy on a woman who suffered from memory loss for years.

Alzheimer’s disease is an irreversible, neurodegenerative disease that affects the brain causing progressive memory loss and destroys thinking skills. Alzheimer’s is the most common type of dementia, which is a general term used to describe disorders that affects brain functions. Alzheimer’s disease is caused by formations of plaques and tangles in the brain. A dangerous protein called beta-amyloid tends to build up over time in the brain. As this protein molecule accumulates, they start to form plaques, which can damage and destroy brain cells. While plaques affect the spaces between the brain cells, an abnormal protein known as “tau” starts affecting inside the brain cell itself. “Tau tangles can interfere with the transportation of nutrients in and out of the cells, causing brain cells to degenerate and die” (Kosik & Bowman, 2015, p. 5). Some common symptoms for Alzheimer’s include memory loss, constantly misplacing things, unable to remember the names of family members, unable to communicate properly, and losing the ability to complete simple daily tasks. Alzheimer’s disease is a fatal disease, but patients don’t die from the disease itself. Advanced Alzheimer’s increases vulnerability and increases the chance of developing infections that soon lead to death.

Main reason for cognition decline could be buildup of plaque and dysfunctional proteins in the brain interfering with neuronal function. Alzheimer’s disease (AD) is an age-related neurodegenerative disease that accounts for more than 60 % of all dementia cases. The disease is characterized by cognitive deficits and memory loss through a process that lead to the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs). This plaque is composed of abnormally hyperphosphorylated tau protein in the brain. Amyloid beta (Aβ or Abeta) is a peptide of 36–43 amino acids, forms amyloid plaques in the brain and are toxic to nerve cells. These peptides result from the amyloid precursor protein (APP), which is cleaved

Alzheimer’s disease: this is most common cause of dementia.Brain cells are surrounded an abnormal protein and internal structure also damaged.In time chemical connection are between brain cells are lost and some cells die. Symptoms may include difficulties with find right words,solving problems,making decision or understand things in three dimension

Alzheimer’s disease is six out of the ten leading causes of death in the U.S. and five out of the ten leading causes of death in elderly people over the age of 65. AD diagnosis occurs through postmortem detection of pathology in neural tissue. The risk of getting AD comes within age. Individuals with MCI are at risk of progression to getting AD. Close to 15 percent of adults above the age 65 are diagnosed with MCI, and more than half of them develop AD more quickly. MCI adults can regain cognitive function by exercising, eating healthy, reducing cholesterol intake, and by working the memory by practicing challenging cognitive tasks. Working memory is a system that underpins cognitive activities ranging from attention to a specific stimulus

However, diseases caused by abnormal prions hold extremely different and fatal implications through the way the immune system responds. Prions when put into a simplistic context are a type of protein which are not perceived as a threat to the human body. These abnormal prions have become miss-folded and this causes them to differ to a normal prion (US National Library of Medicine , 2012) . In the case of a contamination of such prions the Lymphatic system is used as a means of travel with the prion being completely undetected by the immune system. From here onwards it entails a lengthy process to reach the Central Nervous System in a sub sequential order. After entering the lymphatic system the prion proteins attach to the immune cells in our bodies called Follicular Dendritic Cells (FDCs), this causes the prion to replicate by forcing normal prions to miss fold into the same form that causes diseases (Biotechnology and Biological Sciences Research Council, 2014) and in this case Variant Creutzfeldt-Jakob Disease. With the prion having multiplied significantly they travel through axoplasmic transport to the Central Nervous System through the spinal cord and Vagnus nerve, finally reaching the brain where the onset of symptoms will soon begin (Journal of Leukocyte Biology , 2002).The misfolded prions now present in the brain attack and kill neurons

Degenerative diseases are due to aggregation of proteins within specific neurons. These proteins are overproduced as a result of an overactive gene. This process interferes with normal cellular function leading to multiple degenerative diseases and is a field that requires researchers to find treatments.

Neurodegenerative diseases are progressive disorders that mainly affect neuronal cells and functions, and commonly characterized by abnormal protein metabolism and aggregations i.e. Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, Prion diseases, Motor neurone disease, Amyotrophic lateral sclerosis (ALS), Lou Gehrig’s disease, among others. Currently, there is no single cure out there to treat these debilitating diseases. However, present therapies available either slow down the disease progression or inhibit mutant protein’s aggregation. Recent studies are facilitating our understandings in both neurochemistry and the genetic pathogenesis of the disease nature, which may result in exciting new discoveries and also provide a platform for the development of new effective drugs to cure these devastating diseases. This essay will discuss the shared pathological characteristics for common therapeutic approaches to combat against these incapacitating diseases with particular focus on the two most common neurodegenerative diseases: Alzheimer’s and Parkinson’s disease.

Parkinson’s disease (PD) is a progressive and chronic neurodegenerative disorder. It can be characterised clinically by tremor development, bradykinesia, and rigidity (Chaturvedi, 2008). PD is pathologically caused by the loss of dopaminergic neurons in the substantia pars compacta, which regulates motor control, (Magdalena Guerra-Crespo, 2011) with a degeneration of the neurotransmitter dopamine (Wood & Calne, 2011). This disturbance in the movement control centre also decline the presence of laminated inclusions (Lewy bodies) clumped abnormally by protein gene called alpha-synuclein that links to the development of both sporadic, and hereditary cases of PD (Michael J. Fox Foundation, 2012). Both genetic and environmental elements play a role